Mechanistically, we noticed that knockdown of P2X1 in either human primary AML-LICs (Fig. S6I–K) or human AML cell lines (THP-1, U937, MV4-11; Fig. S6L–N) resulted in the significant reduction in the expression levels of BCAT2, BCAT1, MEIS1, HOXA9, PBX1, and PBX3. Furthermore, we had mutated the phosphorylation sites in human AML cell lines and found that neither S387 A nor T389A rescued the impaired leukemogenic activities of the P2X1-knockdown human AML cell lines, such as THP-1 and MV4-11 cells (Fig. S6O, P). The gene discussed is PBX1; the disease is acute myeloid leukemia.